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International Journal of Breast Cancer
Volume 2014 (2014), Article ID 197480, 6 pages
http://dx.doi.org/10.1155/2014/197480
Review Article

Methods of Cell Propulsion through the Local Stroma in Breast Cancer

Canniesburn Plastic Surgery Unit, Glasgow Royal Infirmary, Castle Street, Glasgow G4 0SF, UK

Received 6 January 2014; Accepted 18 March 2014; Published 7 April 2014

Academic Editor: Ian S. Fentiman

Copyright © 2014 Kerry J. Davies. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

In the normal breast, cellular structures change cyclically in response to ovarian hormones. Cell proliferation, apoptosis, invasion, and differentiation are integral processes that are precisely regulated. Normal epithelial cells depend on the formation of intercellular adhesion contacts to form a continuous sheet of stratifying cell layers that are attached to one and other horizontally and vertically. Cells migrate by extending membrane protrusions to explore the extracellular space locating their targets in a chemotactic manner. The formation of cell protrusions is driven by the assembly of actin filaments at the leading edge. Reorganisation is regulated by a highly integrated signalling cascade that transduces extracellular stimuli to the actin filaments. This signalling cascade is governed by GTPases which act as molecular switches leading to actin polymerisation and the formation of filopodia and lamellipodia. This process is linked to downstream molecules known collectively as WASP proteins, which, in the presence of cortactin, form a complex leading to nucleation and formation of branched filaments. In breast cancer, the cortactin is over expressed leading to increased cellular motility and invasiveness. This hugely complex and integrated signalling cascade transduces extracellular stimuli. There are multiple genes related to cell motility which are dysregulated in human breast cancers.